title: Treatment of idiopathic membranous nephropathy.
abstract: Immunosuppressive treatment of patients with idiopathic membranous nephropathy (iMN) is heavily debated. The controversy is mainly related to the toxicity of the therapy and the variable natural course of the disease-spontaneous remission occurs in 40-50% of patients. The 2012 Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Glomerulonephritis provides guidance for the treatment of iMN. The guideline suggests that immunosuppressive therapy should be restricted to patients with nephrotic syndrome and persistent proteinuria, deteriorating renal function or severe symptoms. Alkylating agents are the preferred therapy because of their proven efficacy in preventing end-stage renal disease. Calcineurin inhibitors can be used as an alternative although efficacy data on hard renal end points are limited. In this Review, we summarize the KDIGO guideline and address remaining areas of uncertainty. Better risk prediction is needed to identify patients who will benefit from immunosuppressive therapy, and the optimal timing and duration of this therapy is unknown because most of the randomized controlled trials were performed in low-risk or medium-risk patients. Alternative therapies, directed at B cells, are under study. The discovery of anti-M type phospholipase A2 receptor-antibodies is a major breakthrough and we envisage that in the near future, antibody-driven therapy will enable more individualized treatment of patients with iMN.
authors.affiliation: Department of Nephrology, Radboud University Nijmegen Medical Center, PO Box 9101, 6500 HB, Nijmegen, The Netherlands. j.hofstra@nier.umcn.nl
authors.forename: Julia M
authors.initials: JM
authors.lastname: Hofstra
authors.forename: Fernando C
authors.initials: FC
authors.lastname: Fervenza
authors.forename: Jack F M
authors.initials: JF
authors.lastname: Wetzels
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000627:therapeutic use; D000465:Algorithms; D000477:Alkylating Agents / Q000627:therapeutic use; D000906:Antibodies / Q000032:analysis; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D000963:Antimetabolites / Q000627:therapeutic use; D065095:Calcineurin Inhibitors; D015433:Glomerulonephritis, Membranous / Q000175:diagnosis / Q000188:drug therapy*; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D017410:Practice Guidelines as Topic; D011379:Prognosis; D011507:Proteinuria / Q000517:prevention & control; D054507:Receptors, Phospholipase A2 / Q000276:immunology; D012084:Renin-Angiotensin System; D000069283:Rituximab
chemical_list: D000477:Alkylating Agents; D000906:Antibodies; D058846:Antibodies, Monoclonal, Murine-Derived; D000925:Anticoagulants; D000963:Antimetabolites; D065095:Calcineurin Inhibitors; D005938:Glucocorticoids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007155:Immunologic Factors; D007166:Immunosuppressive Agents; C516360:PLA2R1 protein, human; D054507:Receptors, Phospholipase A2; D000069283:Rituximab; D000324:Adrenocorticotropic Hormone